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PHARMACOLOGY FRCA > MISC DRUGs - > Flashcards

MISC DRUGs - Flashcards

1
Q

where and how is alcohol absorbed?

A

small amiphatic molecule
can cross lipid bilaters with no transporter
20% absorbed from stomach, 80% small intestine via simple diffusion

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2
Q

Vd of ethanol?

A

0.6L/kg

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3
Q

describe the metabolism of alcohol

A

metabolised in the liver and gastric mucosa = 1st pass metabolism

acetate can be converted to acetylcoA and enter krebs

starts as 1st order and then rapidly to 0 order - 1unit/hr

10% is metabolised by CYP2E1 which is upregulated in chronic alchols

can be excreted unchanged by kidneys too
and exhaled

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4
Q

how is the level of alcohol in someone measured?

A

blood alcohol content = most reliable
mass of alchol per volume blood

breathalyser - quick and rapid test
urine alcohol - not v accurate

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5
Q

how does a breathalyser work?

A

original breathalysers are pottasium permanganate = change colour in presence of alcohol

modern uses fuel cells that oxidises ethanol

alcohol crosses pulmonary endothelium and vapourises and is exhaled
BAC correlatates with alveolar conc

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6
Q

what can give a false positive breathalyser test?

A

GORD , mouthwash

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7
Q

how are units calculated

A

1 unit = 10ml or pure alcohol

25ml of 40% = 1unit
1 glass of wine = 2 units
1 pint of beer = 3 units

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8
Q

recommended male and female alcohol intake?

A

women = 14 units/ week
men = 21 units/ week

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9
Q

why do women have a lower recommended alcohol intake than men?

A

lower body water content
slower enzyme pathways

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10
Q

receptor action of alcohol?

A

GABA A allosteric modulation
enhances glutamate activity
dopaminergic activity too

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11
Q

pharmacodynamics of alcohol?

A

ACUTE:
desirable effects - euphoria, mood elevation
CNS - poor judgement, discordination, can lead to sedation
A - aspiration risk and airway obstruction
B - resp depression
C - increased HR and arrhythmias , vasodilation

metabolic - hypoglycaemia, dehydration (ADH)

CHRONIC:
wernickes and korsakoff
CVS disease
liver disease - fatty liver, cirrhosis, varices, coagulopathy
pancreatitis
gastritis

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12
Q

what is the pathogenesis behind alcohol withdrawal?

A

with chronic use GABA downregulation and glutamate upregulation
so without alcohol brain becomes more excitable

hence withdrawal and tolerance develops
tremors, anxiety, insomnia
seizures
delirium tremens

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13
Q

what is wernickes and korsakoff?

A

secondary to thiamine deficiency due to malnutrition and malabsorption

wernickes = encephalopathy, gait ataxia, nystagmus

korsakoff = amnesia and confabulation

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14
Q

how is acute alcohol withdrawal managed?

A

pabrinex - B vitamin mixture to replace thiamine
withdrawal symptoms are scored - GMAWS
benzos given based on this
e.g. chlordiazepoxide, diazepam or lorazepam in liver disease

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15
Q

what screening tools for alcoholics are there?

A

CAGE - cut down, annoyed, guilt, eye opener (first thing you think in morning)

AUDIT questionaire

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16
Q

what is the role of disulfiram

A

inhibits aldehyde dehydrogenase, aldehyde builds up and causes unpleasent effects to reduce drinking.

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17
Q

what is fomepizole

A

Fomepizole is a medication used as an antidote in cases of poisoning from toxic alcohols, primarily ethylene glycol (found in antifreeze) and methanol.

inhibiting the enzyme alcohol dehydrogenase, which is responsible for metabolizing these toxic alcohols into harmful substances.

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18
Q

how do cannibinoids work?

A

contain THC which is the active ingredient with psychoactive effects.
bind cannabinoid receptors - stimulatory initially and then inhibitory

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19
Q

effects of cannabinoids

A

CNS - calmness, anxiety, sedation, dysphoria, psychosis
vasodilation
increased appeptie
effects of smoking - lung cancer, COPD

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20
Q

what are the effects of cocaine?

A

local anaesthetic agent with NA and serotonin reuptake inhibition causing euphoria

acute - tachycardia, euphoria, anxiety, HTN, vasospasm. risk of strokes, MI, seizures.
serotonin syndrome risk
pupil dilation

chronic - IHD and cardiomyopathy, nasal septum perforation

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21
Q

what anaesthetic considerations in someone with cocaine?

A

avoid sympathetic stimulants and serotonin drugs - ephedrine, pethidine, tramadol

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22
Q

how is acute intoxication with cocaine managed?

A

supportive care
may need intubating if reduced GCS
benzos - agitations and seizures
treat complications - nitrates for HTN

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23
Q

how do amphetamines work molecularly ?

A

stimulate the release of dopamine and serotonin causing excitemnet and euphoria

also inhibit MAO

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24
Q

what are the pharmacodynamic effects of amphetamines?

A

euphoria, excitement, energy
CVS - tachycardia and arrhythmias
metabolic - increase ADH and thirst
electrolytes - hyponatraemia - can lead to cererbral oedema
risk of serotonin syndrome

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25
Q

how are ampetamines metabolised?

A

CYP2D6 - genetic variabilty

26
Q

how is acute intoxication of amphetamines managed?

A

supportive
monitor for serotonin signs
thermoregulation
avoid MH triggering drugs eg. sux and volatiles if possible.

27
Q

how do ilicit drugs affect the MAC?

A

acutely - alcohol/ cannabis depresses, amphetamines and cocaine increase

chronic other way round

28
Q

how can recreational drugs be classified?

A

illegal or legal
mechanism - opioid, amphetamines, cannabinoids, benzos, local anaesthetic
stimulants or depressants

29
Q

what are dissociative drugs?

A

hallucinogens - change perception

NMDA antagonists - ketamine
serotonin agonist - LSD

30
Q

what anaesthetic considerations would you make with someone with substance abuse?

A
  • Difficult IV access
  • downregulation of enzymes / higher MAC
  • nutritional deficiency
  • withdrawal symptoms
  • difficult analgesic management
31
Q

what are the components in cigarrete smoke?

A

CO, nicotine, tar

32
Q

pharmacodynamic effects of nicotine?

A

similar in structure to ACh, binds nACHR
also increases dopamine, serotonin and endorphins

overall - tachycardia, increased BP, alertness, mood elevation , addiction , appetite supression

33
Q

what are the harmful effects of smoking?

A

tar - lung cancer and COPD
CO - carboxyHb
increased risk of IHD + MI

increases MAC , reduces PONV

34
Q

describe the effect of CO on O2 carriage

A

CO binds Hb with much higher affinity and blocks O2 bidning sites.
also conformational change that increases affinity of sites already bound to O2 so less release. - left shift.

35
Q

how would you manage someone who smoked for general anaesthesia?

A

Pre op - if time, ask if they can stop , the longer the period of cessation the better.

regional if possible
avoid bronchospasm agents - atracurium, morphine

36
Q

what is the mechanism of bupropion and verenicline (champix)

A

bupropion = nicotine receptor antagonist + dop reuptake inhibitor + adrenergic actions

verenicline = nAChR partial agonist

37
Q

side effects of bupropion

A

seizures
cant be used in preg / breast feeding

38
Q

side effects of verenicline?

A

nausea and headaches
vivid dreams
suicidal ideation
not in preg and breastfeeding

39
Q

describe the pathophysiology of acute asthma…

A

chronic condition with episodic small airway constriction , mucus secretion and inflammation.

results in wheeze, SoB and cough - diurnal variation

triggered by e.g. cold, dust, viral infection

can lead to type 1 resp failure and with exhaustion type 2

40
Q

how is acute asthma classified?

A

severe - PEFR 33-50%, RR >25, HR >110
life threatening - 33,92, CHEST - PEFR 33, 92% sats, Cyanosis, hypotension, exhaustion , silent chest, tachyarrhythmia
near fatal - rise in CO2

41
Q

how is chronic asthma managed?

A

SABA - short acting B agonists - salbutamol
step 1 - Steroid inhaler
step 2 - LABA - salmeterol
step 3 - switch to leukotriene receptor antagonist (montelukast) or increase steroid

other - theophylline, LAMA , biologics

42
Q

risk factors for near fatal asthma?

A

previous episode
previous admission
uncontrolleed asthma

43
Q

how is life threatening asthma managed?

A

A to E
sit them up and forward
15L non rebreathe
salbutamol (5mg) , ipratropium nebs (500ug)
steroid - hydrocorisone IV or prednisolone 40mg
MgSO4

IV aminophylline
adrenaline nebs

other - ketamine, sevo, heliox, intubation

44
Q

how is aminophylline given?

A

loading dose 5mg/kg
plus infusion
if on theophylline avoid loading dose

45
Q

which anaesthetic drugs should be avoided in asthma?

A

atracurium
morphine
thiopentone
B blockers
NSAIDs

46
Q

which drugs act as bronchodilators?

A

These can be classed by mechanism of action

B agonists - GPCR - promotes smooth muscle relaxation.
- short acting - salbutamol , terbutaline
- long acting - salmeterol

antimuscarinics - M3 - Gq -normally increases Ca, inhibition of these increases relaxation
- ipratropium and tiotropium

Phosphodiesterase inhibitors - aminophylline, thiophylline

misc - ketamine, MgSO4, inhalation agents

47
Q

tell me about salbutamol

A

synthetic agonist at B2 receptors
comes as IV, Inhaled form, oral tablet and nebulisers
used for COPD and asthma and hyperkalaemia treatment

effects:
- bronhcodilation
- also B1 - tachycardia , tremor
- B2 - vasodilation and hypotension
- hypokalaemia
- lactic acidosis

kinetics
- orally but extensive 1st pass
- hepatic and renal

48
Q

tell me about ipratropium bromide..

A

muscarinic antagonist
used in acute and chronic asthma management and COPD
comes as inhaler or nebuliser

effects
bronchodilation via blocking parasympathetic mediated bronchoconstrictiom.
however also has systemic effects - tachycardia, dry mouth, can exacerbate glaucoma

49
Q

tell me about aminophylline..

A

phosphodiesterase inhibitor
used in acute asthma attacks and as an ionotrope in cardiogenic shock.

can be given as IV with loading dose of 5mg/kg and then infusion. usually in HDU or ITU as needs monitoring due to CVS effects.
also available in tablet form.

mechansims - increases cAMP - PKA - inactivation of MLCK and less Ca into cell.

dynamics
- bronchodilation
- ionotrophic and chronotrophic efects

kinetics
- good BO
- quick to have 0 order kinetics and narrow therapeutic index - needs monitoring.

50
Q

how do leukotriene receptor anatagonists help asthma?

A

montelukast
inhibits GPCR invovled in mediating inflammation
used for long term asthma management

51
Q

what is surfactant? how is it used clinically?

A

naturally occuring lipoprotein comple with amiphatic properties
used to reduced surface tension of alveoli to improve compliance

can be used in neonatal acutre resp distress syndrome - given exogenously via ET tube.

52
Q

what drugs can be used to treat pulmonary HTN?

A

endothelin antagonist - bosentan - oral
thromboxane A2 antagonists - nebulised
phosphodiesterase inhibitors - sildenafil
prostacyclin
inhaled NO

53
Q

causes of pulmonary artery hypertension?

A

chronic hypoxia - e.g. altitude or lung disease
chronic thromboembolitic disease
left heart disease
idiopathic

54
Q

what is doxapram?

A

stimulates the respiratory centre
can be used post anaesthetic to help with breathing however causes feeling of breathlessness, tachycardia and panic

55
Q

what drugs can be used to improve minute ventilation?

A

depends on the cause
doxapram, naloxone, flumezanil

56
Q

do you know any drugs that cause lung injury?

A

chemotherapy agents - bleomycin , methotrexate
amiodarone
oxygen

57
Q

what is histamine?

A

naturally occuring amine
important hormone and neurotransmitter
involved in immunity, nervous system, GIT

acts on histamine receptors - H1 - 4 exist.

effects:
- CNS - sedation , role in emesis
- CVS - vasodilation, tachycardia
- GI - gastric secretions and motility
- resp - bronchoconstriction
- immune - itching, rash

58
Q

what histamine receptors do you know?

A

Histamine receptors are GPCRs and fall into 4 categories

H1 - many organs, CNS, smooth muscle, endothelium and respiratory tract. GPCR Gq

H2 - GI tract - gastric secretions and motility. GPCR Gs

H3 - CNS - Gi
H4 - immune role - Gi

59
Q

what antihistamines do you know?

A

anti-histamines block H1 receptors.
they are implicated in N&V, sedation, allergy

they act via inverse antagonism of H1

can be classed into 3 groups
1st generation - cyclizine, chlorphenamine
2nd generation - loratidine, cetrizine
3rd gen - fexofenadine

in general the 1st gen cross BBB more readily and have more sedative effects.

60
Q
A

PHARMACOLOGY FRCA (16 decks)

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